Hepatitis grave producida por intoxicación con té verde en un niño. Presentación de un caso / Severe hepatitis caused by green tea intoxication in a child. Case report

El daño hepático inducido por hierbas es una reacción adversa relacionada con el uso de medicina herbaria, incluida en el grupo de daño hepático inducido por drogas. El uso terapéutico de hierbas medicinales es cada vez más frecuente por la creencia de que los productos naturales o hierbas son siempre seguros. En Estados Unidos, la incidencia de toxicidad alcanza un 9 % y, en países de Asia, un 19-63 % de los casos totales de daño hepático inducido por drogas.El té verde es obtenido de las hojas de la Camellia sinensis. Las hojas recién cosechadas son estabilizadas por calentamiento en seco para inactivar la enzima polifenol y luego se secan rápidamente. Su consumo ha aumentado en los últimos años, y se han documentado reacciones hepatotóxicas. Se presenta un caso de hepatitis aguda grave asociada al consumo de té verde en un niño de 2 años.

Herb-induced liver injury is a type of adverse drug reaction related to using herbal medicine, and now is a segment of drug-induced liver injury. The use of herbal products has increased significantly, because it is generally regarded as safe and natural by the public. In the United States, the incidence reaches 9 % and, in the countries of Asia, 19-63 % of the total cases of drug-induced liver injury. Green tea is obtained from the leaves of the Camellia sinensis. Freshly harvested leaves are stabilized by dry heating to inactivate the polyphenol enzyme and then dried quickly. Its consumption has increased in recent years and has been reported with hepatotoxic reactions.We present a case of severe hepatitis related to the consumption of green tea in a 2-year-old child.

[Severe hepatitis caused by green tea intoxication in a child. Case report]. / Hepatitis grave producida por intoxicación con té verde en un niño. Presentación de un caso.

Herb-induced liver injury is a type of adverse drug reaction related to using herbal medicine, and now is a segment of druginduced liver injury. The use of herbal products has increased significantly, because it is generally regarded as safe and natural by the public. In the United States, the incidence reaches 9 % and, in the countries of Asia, 19-63 % of the total cases of druginduced liver injury. Green tea is obtained from the leaves of the Camellia sinensis. Freshly harvested leaves are stabilized by dry heating to inactivate the polyphenol enzyme and then dried quickly. Its consumption has increased in recent years and has been reported with hepatotoxic reactions. We present a case of severe hepatitis related to the consumption of green tea in a 2-year-old child.

El daño hepático inducido por hierbas es una reacción adversa relacionada con el uso de medicina herbaria, incluida en el grupo de daño hepático inducido por drogas. El uso terapéutico de hierbas medicinales es cada vez más frecuente por la creencia de que los productos naturales o hierbas son siempre seguros. En Estados Unidos, la incidencia de toxicidad alcanza un 9 % y, en países de Asia, un 19-63 % de los casos totales de daño hepático inducido por drogas. El té verde es obtenido de las hojas de la Camellia sinensis. Las hojas recién cosechadas son estabilizadas por calentamiento en seco para inactivar la enzima polifenol y luego se secan rápidamente. Su consumo ha aumentado en los últimos años, y se han documentado reacciones hepatotóxicas. Se presenta un caso de hepatitis aguda grave asociada al consumo de té verde en un niño de 2 años.

El hígado y la toxicidad por drogas, hierbas y suplementos dietéticos / Drug-, herb- and dietary supplement-induced liver injury

El daño hepático por drogas y sustancias representa, aproximadamente, el 20% de los casos de falla hepática aguda en niños. Está causada por dos mecanismos: hepatotoxicidad directa y por idiosincrasia. La primera surge de la administración de una droga con toxicidad intrínseca y es dependiente de la dosis (ejemplo: acetaminofén). La idiosincrasia es impredecible, ocurre con baja frecuencia, es variable en su presentación y no depende de la dosis. Las manifestaciones clínicas, histológicas y de laboratorio son hepatitis, en general, asintomática, con gran aumento de enzimas hepáticas; colestasis, con ictericia, prurito, aumento predominante de fosfatasa alcalina y leve aumento de aminotransferasas; o mixto, hepatitis más colestasis. El tiempo de recuperación es variable, ya que depende del tipo de daño hepático. La detección temprana y la suspensión precoz de la droga son las intervenciones más eficaces e importantes para acelerar la resolución histológica y clínica, y reducir el daño hepático grave.

Drug- and substance-induced liver injury accounts for approximately 20% of pediatric cases of acute liver failure. It is caused by two mechanisms: direct and idiosyncratic hepatotoxicity. Direct hepatotoxicity is the result of the administration of a drug with intrinsic toxicity and is dose-dependent (e.g., acetaminophen). Idiosyncratic hepatotoxicity is unpredictable, uncommon, variable in presentation, and doseindependent. The clinical, histological, and laboratory manifestations include hepatitis, which is generally asymptomatic but with a significant increase of liver enzymes; cholestasis, accompanied with jaundice, pruritus, prominent elevation of alkaline phosphatase, and mild elevation of aminotransferases; or mixed, with elements of both hepatitis and cholestasis. Time to recovery is variable, depending on the type of liver injury. Early detection and discontinuation of the causative drug is the most effective and important step for the fast resolution of histological and clinical changes, thus reducing severe liver injury.

Drug-, herb- and dietary supplement-induced liver injury. / El hígado y la toxicidad por drogas, hierbas y suplementos dietéticos.

Drug- and substance-induced liver injury accounts for approximately 20% of pediatric cases of acute liver failure. It is caused by two mechanisms: direct and idiosyncratic hepatotoxicity. Direct hepatotoxicity is the result of the administration of a drug with intrinsic toxicity and is dose-dependent (e.g., acetaminophen). Idiosyncratic hepatotoxicity is unpredictable, uncommon, variable in presentation, and doseindependent. The clinical, histological, and laboratory manifestations include hepatitis, which is generally asymptomatic but with a significant increase of liver enzymes; cholestasis, accompanied with jaundice, pruritus, prominent elevation of alkaline phosphatase, and mild elevation of aminotransferases; or mixed, with elements of both hepatitis and cholestasis. Time to recovery is variable, depending on the type of liver injury. Early detection and discontinuation of the causative drug is the most effective and important step for the fast resolution of histological and clinical changes, thus reducing severe liver injury.

El daño hepático por drogas y sustancias representa, aproximadamente, el 20% de los casos de falla hepática aguda en niños. Está causada por dos mecanismos: hepatotoxicidad directa y por idiosincrasia. La primera surge de la administración de una droga con toxicidad intrínseca y es dependiente de la dosis (ejemplo: acetaminofén). La idiosincrasia es impredecible, ocurre con baja frecuencia, es variable en su presentación y no depende de la dosis. Las manifestaciones clínicas, histológicas y de laboratorio son hepatitis, en general, asintomática, con gran aumento de enzimas hepáticas; colestasis, con ictericia, prurito, aumento predominante de fosfatasa alcalina y leve aumento de aminotransferasas; o mixto, hepatitis más colestasis. El tiempo de recuperación es variable, ya que depende del tipo de daño hepático. La detección temprana y la suspensión precoz de la droga son las intervenciones más eficaces e importantes para acelerar la resolución histológica y clínica, y reducir el daño hepático grave.

Pediatric hospitalizations associated with 2009 pandemic influenza A (H1N1) in Argentina.

BACKGROUND: While the Northern Hemisphere experiences the effects of the 2009 pandemic influenza A (H1N1) virus, data from the recent influenza season in the Southern Hemisphere can provide important information on the burden of disease in children. METHODS: We conducted a retrospective case series involving children with acute infection of the lower respiratory tract or fever in whom 2009 H1N1 influenza was diagnosed on reverse-transcriptase polymerase-chain-reaction assay and who were admitted to one of six pediatric hospitals serving a catchment area of 1.2 million children. We compared rates of admission and death with those among age-matched children who had been infected with seasonal influenza strains in previous years. RESULTS: Between May and July 2009, a total of 251 children were hospitalized with 2009 H1N1 influenza. Rates of hospitalization were double those for seasonal influenza in 2008. Of the children who were hospitalized, 47 (19%) were admitted to an intensive care unit, 42 (17%) required mechanical ventilation, and 13 (5%) died. The overall rate of death was 1.1 per 100,000 children, as compared with 0.1 per 100,000 children for seasonal influenza in 2007. (No pediatric deaths associated with seasonal influenza were reported in 2008.) Most deaths were caused by refractory hypoxemia in infants under 1 year of age (death rate, 7.6 per 100,000). CONCLUSIONS: Pandemic 2009 H1N1 influenza was associated with pediatric death rates that were 10 times the rates for seasonal influenza in previous years.